The Effective Pollination Period of European Plum (Prunus domestica L.) Cultivars in Western Norway

This study evaluated the effective pollination period (EPP) in four European plum (Prunus domestica L.) cultivars (‘Mallard’, ‘Edda’, ‘Jubileum’, and ‘Reeves’) during two years (2018–2019) under the environmental conditions in western Norway. The pollination of plum cultivars was carried out one, three, five, seven, and nine days after anthesis (DAA) with a pollen mix of two compatible cultivars (‘Victoria’ and ‘Opal’). Initial, middle-season, and final fruit set was recorded after one month and two months after pollination and just before the harvest, respectively. On average from both years cultivar ‘Jubileum’ had the highest fruit set when pollinated one, three, five, seven, and nine DAA (33.23%, 30.83%, 8.47%, 3.08%, and 1.15%, respectively), which was more than two folds higher fruit set than in the other studied cultivars. Cultivar ‘Jubileum’ showed significantly reduced fruit set between pollination on five and nine DAA, while cultivars ‘Mallard’, ‘Edda’, and ‘Reeves’ had markedly reduced fruit set if pollinated three to five DAA, implying that the EPP in ‘Jubileum’ was five days while in the rest it was three days. Variation of weather conditions during the flowering period in both years did not have a major effect on the receptivity of stigmas in the studied plum cultivars, which means that the existing differences in the length of EPP is maternal-genotype dependent.

Introgressions of Vitis rotundifolia Michx. to obtain grapevine genotypes with complex resistance to biotic and abiotic stresses

Vitis rotundifolia Michx. is one of the species of the family Vitaceae, with resistance to both biotic and abiotic stresses. The present study reports new scientific knowledge about the inheritance of resistance to downy mildew, powdery mildew and frost by V. vinifera varieties from V. rotundifolia. Recombinant lines of three hybrid populations from the crossing of the maternal genotype ♀M. 31-77-10 with V. rotundifolia hybrids were used as the object of the study. As a result of laboratory screening, more than 40 % of recombinants of the ♀M. 31-77-10× ×[DRX-M5-734+DRX-M5-753+DRX-M5-790] population showed a high degree of frost resistance (–24 °C), while 6 % of transgressive recombinants were characterized by a very high degree of resistance (–27 °С). The maternal genotype ♀M. 31-77-10 does not carry alleles of resistance to powdery mildew at the Run1 locus and in the field suffers from powdery mildew much more than the paternal genotypes. The prevalence of powdery mildew on vegetative organs in the three recombinant populations over the years varies on average between 3.2–17.1, 0.3–17.7 and 0.6–5.2 %, respectively. As a result, almost all recombinant genotypes that received a resistant allele from the paternal genome are highly resistant to powdery mildew.

Do Genetic Variants Modify the Effect of Smoking on Risk of Preeclampsia in Pregnancy?

Objective Maternal smoking is associated with as much as a 50% reduced risk of preeclampsia, despite increasing risk of other poor pregnancy outcomes that often co-occur with preeclampsia, such as preterm birth and fetal growth restriction. Researchers have long sought to understand whether this perplexing association is biologically based, or a result of noncausal mechanisms. We examined whether smoking-response genes modify the smoking-preeclampsia association to investigate potential biological explanations. Study Design We conducted a nested case–control study within the Norwegian Mother, Father and Child Birth Cohort (1999–2008) of 2,596 mother–child dyads. We used family-based log-linear Poisson regression to examine modification of the maternal smoking-preeclampsia relationship by maternal and fetal single nucleotide polymorphisms involved in cellular processes related to components of cigarette smoke (n = 1,915 with minor allele frequency ≥10%). We further investigated the influence of smoking cessation during pregnancy. Results Three polymorphisms showed overall (p < 0.001) multiplicative interaction between smoking and maternal genotype. For rs3765692 (TP73) and rs10770343 (PIK3C2G), protection associated with smoking was reduced with two maternal copies of the risk allele and was stronger in continuers than quitters (interaction p = 0.02 for both loci, based on testing 3-level smoking by 3-level genotype). For rs2278361 (APAF1) the inverse smoking-preeclampsia association was eliminated by the presence of a single risk allele, and again the trend was stronger in continuers than in quitters (interaction p = 0.01). Conclusion Evidence for gene–smoking interaction was limited, but differences by smoking cessation warrant further investigation. We demonstrate the potential utility of expanded dyad methods and gene–environment interaction analyses for outcomes with complex relationships between maternal and fetal genotypes and exposures. Key Points

Understanding etiology of chromosome 21 nondisjunction from gene × environment models

Maternal risk factors and their interactions with each other that associate chromosome 21 nondisjunction are intriguing and need incisive study to be resolved. We determined recombination profile of nondisjoined chromosome 21 and maternal genotypes for four selected polymorphic variants from the folate regulators genes stratifying the women according to the origin of segregation error and age at conception. We conducted association study for genotype and maternal addiction to smokeless chewing tobacco, usually chopped tobacco leaves or paste of tobacco leaves with the incidence of Down syndrome birth. Additionally, we designed various logistic regression models to explore the effects of maternal genotype, maternal habit of smokeless chewing tobacco, maternal age at conception and all possible interactions among them on chromosome 21 nondisjunction. We found folate regulator gene mutations are associated with maternal meiosis II error. Regression models revealed smokeless chewing tobacco and folate polymorphic/mutant risk genotype interact with each other to increase the risk of reduced and single peri-centromeric recombination events on chromosome 21 that nondisjoined at meiosis II in the oocytes and the effect is maternal age independent. We inferred maternal folate polymorphic/mutant risk genotypes and habit of smokeless chewing tobacco interact with each other and increase the risk of meiosis II error in oocytes in maternal age-independent manner.

P.090 Evaluation of Mutant Alleles of Engrailed and Invected in Drosophila Melanogaster Models of Parkinson Disease

Background: Parkinson Disease (PD) is a neurodegenerative disorder, resulting in a gradual decline in voluntary movement, where lifespan remains stable. Drosophila melanogaster offer comparable gene sequences to those targeted in PD; among them are two transcription factors, engrailed (en) and invected (inv). Methods: Wild-type homozygous allele Oregon-R(en+, inv+) was compared to heterozygous mutants of en1, en4, en7, en54, en58, invW, inv30, and Df (2R) enEinvE. Nine climbing and aging studies were executed from crosses with w1118(en+, inv+) as the maternal genotype. Results: Independent-samples t-tests were conducted to compare the percent survival (in days). No significant differences were observed between the experimental groups and the control group. A mixed Analysis of Variance was conducted to compare climbing behaviour over time (in weeks) for all nine groups. Both main effects (group, time), and the interaction (group x time) were significant. Post hoc Fisher’s Least Significant Difference tests revealed a significant difference between the control group and en1, en4, en54, invW, and Df (2R) enEinvE groups. Conclusions: These results support the hypothesis that mutations of en, inv, or both will result in a PD phenotype and consequent decreased motor function of D. melanogaster PD models, with or without a significant decrease in lifespan.

Neurogenic Plasticity in a Serotonin Transporter Knockout Model: Effects of Maternal and Offspring Genotype

<p>Major depressive disorder (MDD) is debilitating mental disorder that is increasing in prevalence. Many theories have tried to explain the aetiology of depression including the classic monoamine deficiency hypothesis and the newer neurogenic hypothesis. The finding that selective serotonin transporter inhibitors (SSRIs) work by increasing extracellular serotonin levels in the brain and have antidepressant effects has formed the basis of the most widely accepted theory of depression, the monoamine hypothesis. However, a genetic reduction in human and animal serotonin reuptake transporters, which also increases extracellular serotonin, is associated with depressive symptomology. This paradox is not explained by the monoamine hypothesis. The key difference between these two scenarios is that genetically induced increases in serotonin occur from development onward, while SSRIs increase serotonin only in adulthood. Furthermore, SSRIs typically take several weeks to confer a therapeutic effect. This finding has led to the hypothesis that, rather than acute monoamine-increasing effects, it is the downstream effects of such increases on neurogenesis and neural plasticity which confer antidepressant effects. To further elucidate the neurobiology of depression, this study sought to examine the effects of genetically increasing serotonin on early postnatal neurogenesis in a serotonin knockout rat model using BrdU immunohistochemistry. We examined both the offspring and maternal genotype effects. We found that SERT-/- offspring had the highest levels of neurogenesis compared with SERT+/- and SERT+/+ at postnatal day 7. In addition we found a maternal genotype effect with SERT+/+ offspring born and reared by SERT+/- mothers having lower neurogenesis compared to SERT+/+ offspring from SERT+/+ mothers. The potential effects of maternal caregiving, neuroplasticity in altered mood and stress responses and the role of 5-HT receptors are discussed.</p>

Neurogenic Plasticity in a Serotonin Transporter Knockout Model: Effects of Maternal and Offspring Genotype

<p>Major depressive disorder (MDD) is debilitating mental disorder that is increasing in prevalence. Many theories have tried to explain the aetiology of depression including the classic monoamine deficiency hypothesis and the newer neurogenic hypothesis. The finding that selective serotonin transporter inhibitors (SSRIs) work by increasing extracellular serotonin levels in the brain and have antidepressant effects has formed the basis of the most widely accepted theory of depression, the monoamine hypothesis. However, a genetic reduction in human and animal serotonin reuptake transporters, which also increases extracellular serotonin, is associated with depressive symptomology. This paradox is not explained by the monoamine hypothesis. The key difference between these two scenarios is that genetically induced increases in serotonin occur from development onward, while SSRIs increase serotonin only in adulthood. Furthermore, SSRIs typically take several weeks to confer a therapeutic effect. This finding has led to the hypothesis that, rather than acute monoamine-increasing effects, it is the downstream effects of such increases on neurogenesis and neural plasticity which confer antidepressant effects. To further elucidate the neurobiology of depression, this study sought to examine the effects of genetically increasing serotonin on early postnatal neurogenesis in a serotonin knockout rat model using BrdU immunohistochemistry. We examined both the offspring and maternal genotype effects. We found that SERT-/- offspring had the highest levels of neurogenesis compared with SERT+/- and SERT+/+ at postnatal day 7. In addition we found a maternal genotype effect with SERT+/+ offspring born and reared by SERT+/- mothers having lower neurogenesis compared to SERT+/+ offspring from SERT+/+ mothers. The potential effects of maternal caregiving, neuroplasticity in altered mood and stress responses and the role of 5-HT receptors are discussed.</p>

Acropetal and basipetal cardenolide transport in Erysimum cheiranthoides (wormseed wallflower)

Plant specialized metabolites are often subject to within-plant transport and have tissue-specific distribution patterns. Among plants in the Brassicaceae, the genus Erysimum is unique in producing not only glucosinolates but also cardenolides as defense against insect herbivory. Ten cardenolides were detected with varying abundance in different tissues of Erysimum cheiranthoides (wormseed wallflower). As is predicted by the optimal defense theory, cardenolides were most abundant in young leaves and reproductive tissues. The lowest concentrations were observed in senescing leaves and roots. Crosses between wildtype E. cheiranthoides and a mutant line with an altered cardenolide profile showed that the seed cardenolide phenotype is determined entirely by the maternal genotype. Prior to the development of the first true leaves, seedling cotyledons also had the maternal cardenolide profile. Hypocotyl grafting experiments showed that the root cardenolide profile is determined entirely by the aboveground plant genotype. In further grafting experiments, there was no evidence of cardenolide transport into the leaves, but a mixed cardenolide profile was observed in the stems and inflorescences of plants that had been grafted at vegetative and flowering growth stages, respectively. Together, these results indicate that E. cheiranthoides leaves are a site of cardenolide biosynthesis and therefore also the plant tissue that is most likely to be expressing the relevant biosynthetic genes.

Impacts of Maternal Genotype on Pecan Seedling Performance in an Alkaline, Saline-sodic Soil

A field study was conducted to evaluate tolerance of pecan rootstocks to soil salinity and sodicity. Seven cultivars—Elliott, Giles, Ideal, Peruque, Riverside, ‘Shoshoni, and VC1-68—were selected from a range of geographic regions of origin. The soil of the experimental plot was a poorly drained, saline–sodic Pima silty clay variant. The irrigation water was a moderately saline mix of Gila River and local groundwater with an electrical conductivity of 2.8 dS⋅m–1, containing primarily ions of Na and Cl. Eighty seeds of each cultivar were planted in a greenhouse in late Feb. 2016; 48 seedlings of each cultivar were transplanted into field plots in Feb. 2017. Half the trees received a soil-based application of Zn–ethylenediaminetetraacetic acid (EDTA) at planting. The trees were observed and rated for both vigor and resistance to salt injury on seven separate occasions. Trunk diameter was measured each dormant season. Leaf samples were collected on 9 Oct. 2019 and 6 Oct. 2020, and were analyzed for nutrient content. Zn-EDTA was not found to have a significant effect on growth, vigor, or resistance to salt injury. ‘Elliott’ seedlings exhibited greater tolerance for the alkaline, saline–sodic soil conditions than other cultivars. ‘Giles’ and ‘Peruque’ were most severely affected. Resistance to salt injury (ranging from marginal leaf burn to necrosis of entire leaf), vigor, and growth correlated more strongly with foliar concentrations of Na than Cl or K during 2019. Vigor and growth were not significantly correlated with foliar Na, Cl, or K concentrations in 2020. The foliar K:Na ratio had a nearly equal correlation with resistance to salt injury and a greater correlation with growth than that of Na alone in 2019. However, although the correlation of the K:Na ratio with vigor was stronger than that of Cl or K, Na had the strongest correlation with vigor in 2019. In 2020, the only significant correlation of growth and vigor was with the K:Na ratio. The strongest correlation with resistance to salt injury in 2020 was with foliar Na concentration.